Irem Soyler
About
My research project
Microbial responses to high frequency ultrasound in food relevant systemsMy PhD project investigates the antimicrobial mechanisms and potential unintended consequences of high frequency ultrasound as a non thermal food preservation technology. While ultrasound is increasingly promoted as a sustainable alternative to conventional thermal treatments, its ability to induce sublethal stress responses in bacteria remains poorly understood. This project aims to characterise how ultrasound mediated physical and chemical effects influence bacterial inactivation, stress adaptation, and regrowth behaviour in food relevant microorganisms. The work focuses primarily on Escherichia coli and Listeria monocytogenes, including wild type and stress response mutant strains, to elucidate the role of oxidative stress, heat generation, and mechanical disruption during ultrasonic exposure.
In addition, the project explores combination treatments with natural antimicrobials such as green tea extract and epigallocatechin gallate to evaluate synergistic or protective effects under ultrasonic conditions. By integrating engineering characterisation with microbiological and mechanistic analyses, this research provides critical insight into whether ultrasound promotes safe microbial inactivation or inadvertently enhances bacterial stress tolerance. The findings aim to inform the responsible application of ultrasound in food processing and contribute to evidence based non thermal preservation strategies.
Supervisors
My PhD project investigates the antimicrobial mechanisms and potential unintended consequences of high frequency ultrasound as a non thermal food preservation technology. While ultrasound is increasingly promoted as a sustainable alternative to conventional thermal treatments, its ability to induce sublethal stress responses in bacteria remains poorly understood. This project aims to characterise how ultrasound mediated physical and chemical effects influence bacterial inactivation, stress adaptation, and regrowth behaviour in food relevant microorganisms. The work focuses primarily on Escherichia coli and Listeria monocytogenes, including wild type and stress response mutant strains, to elucidate the role of oxidative stress, heat generation, and mechanical disruption during ultrasonic exposure.
In addition, the project explores combination treatments with natural antimicrobials such as green tea extract and epigallocatechin gallate to evaluate synergistic or protective effects under ultrasonic conditions. By integrating engineering characterisation with microbiological and mechanistic analyses, this research provides critical insight into whether ultrasound promotes safe microbial inactivation or inadvertently enhances bacterial stress tolerance. The findings aim to inform the responsible application of ultrasound in food processing and contribute to evidence based non thermal preservation strategies.
Publications
The antimicrobial mechanisms of high-frequency ultrasound (HFUS) under low-power conditions were investigated using Escherichia coli as a model foodborne pathogen, with oxidative and physical contributions evaluated through radical scavenger assays, intracellular ROS quantification, flow cytometry, and scanning electron microscopy. Bacterial inactivation was strongly frequency-dependent. 760 kHz induced greater intracellular ROS accumulation and membrane permeabilisation than 500 kHz, and radical scavenger experiments confirmed a major ROS contribution to inactivation. The combination of HFUS (760 kHz, 30 W) with epigallocatechin gallate (EGCG; 0.2 mg/mL) produced synergistic antibacterial efficacy, accompanied by enhanced membrane depolarisation, permeabilisation, and ultrastructural damage. Pre-exposure to ultrasound increased bacterial sensitivity to subsequent lethal thermal (56°C) and oxidative (10 mM H2O2) challenges. Mutant analysis of eight E. coli K-12 strains revealed that antioxidant defence systems, particularly glutathione reductase (gor), were critical for survival, while deletion of the general stress regulator rpoS or oxidoreductase grxA increased tolerance, indicating complex interacting stress-response mechanisms. Overall, HFUS inactivation is driven primarily by a combination of chemical and physical mechanisms, encompassing ROS-mediated oxidative damage and cavitation-induced membrane disruption, enhancing bacterial susceptibility to additional antimicrobial stresses, and therefore holds greater potential as a complementary technology than as a stand-alone treatment.